Root K V, Engelhardt J F, Post M, Wilson J W, Van Dyke R W
Dept. Internal Medicine and Cystic Fibrosis Center, Univ. Michigan, Ann Arbor 48109-0682.
Biochem Biophys Res Commun. 1994 Nov 30;205(1):396-401. doi: 10.1006/bbrc.1994.2678.
Endosomes from L cells, transduced with the CFTR gene, and the parental line, which does not express detectable levels of CFTR, were loaded with FITC-dextran, isolated and the initial rates of acidification, steady-state pHi, and proton leak rates were compared over a range of chloride concentrations (0-140 mM). Values for these parameters were similar for endosomes from both cell lines in the presence and absence of cAMP and PKA. These results indicate that CFTR does not alter L cell endosome acidification, possibly due to an adequate intrinsic CI- conductance or to a failure to incorporate sufficient functional CFTR or a necessary co-factor in endocytic membranes.
用CFTR基因转导的L细胞的内体，以及不表达可检测水平CFTR的亲代细胞系，用FITC-葡聚糖加载，分离后，在一系列氯化物浓度（0-140 mM）范围内比较酸化的初始速率、稳态细胞内pH值和质子泄漏率。在有和没有cAMP和PKA的情况下，两种细胞系内体的这些参数值相似。这些结果表明，CFTR不会改变L细胞内体的酸化，这可能是由于足够的内在氯离子电导，或者是由于未能在胞吞膜中掺入足够的功能性CFTR或必需的辅助因子。
